p38 Kinase and c‐Jun N‐Terminal Kinase Oppositely Regulates Tumor Necrosis Factor α‐Induced Vascular Cell Adhesion Molecule‐1 Expression and Cell Adhesion in Chondrosarcoma Cells

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Abstract
We investigated signaling pathways leading to tumor necrosis factor (TNF) α‐induced intercellular adhesion molecule (ICAM)‐1 and vascular cell adhesion molecule (VCAM)‐1 expression in chondrosarcoma cells, and determined the functional significance of their expression by examining Jurkat T cell adhesion. TNF αinduced VCAM‐1 and ICAM‐1 expression and Jurkat T cell binding. Antibody blocking assay indicated that VCAM‐1 mediates TNF α‐induced Jurkat T cell adhesion. TNF αcaused activation of mitogen‐activated protein (MAP) kinase subtypes, extracellular signal‐regulated protein kinase, p38 kinase, and c‐jun N‐terminal kinase (JNK). ICAM‐1 expression was not altered by the inhibition of MAP kinases. However, VCAM‐1 expression and Jurkat T cell adhesion was blocked by the inhibition of p38 kinase, whereas inhibition of JNK enhanced VCAM‐1 expression and cell adhesion without any modulation of NF κB activation. Our results, therefore, indicate that p38 kinase mediates TNF α‐induced VCAM‐1 expression and cell adhesion, whereas JNK suppresses VCAM‐1 expression that is independent to NF κB activation.

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